Welcome back. We're going to discuss pressure changes and resistance. We will talk specifically about the changes in pressure that occur when we breathe. Then we will also consider resistance of the airways and how that will affect the amount of air that we get into our lungs. So to start off we need to go back to the anatomy of the respiratory system, where we said that we have our lungs in the chest cavity. We said that if the chest wall expands, then the lungs will expand, as well. The explanation for that, is because we have the pleural sac. The inner layer of the pleural sac is attached to the lung. That's right here. The outer layer is attached to the chest wall. In between, we have fluid. This arrangement means that whatever happens to the chest wall the lungs will follow. You can think of this example. If you have two glass slides, or two glass plates and you put some water in between them. You will be to slide them along each other very easily. But to pry them apart gets really difficult, again because of the surface tension of water. So that's how this fluid in the pleural sac functions. It allows for there to be no friction between the lungs and the chest wall, but yet it keeps the lungs next to the chest wall. That's the function of the pleural sac. Now that we've talked about that, we can consider the pressure in the pleural sac. So we've got a few things marked here, where we've got the pressure, atmospheric pressure. Which we're going to just assume is zero. We know it's really equal to 760 millimeters of mercury, but for ease of computations we will call it zero millimeters of mercury. And we've already talked about the pressure in the alveoli, which is gonna be P capital A, P big A. So we're just kind of considering the pressure in the lungs in general in this diagram. Then we've got the chest wall and the intrapleural fluid. That fluid in the plural sac between the lungs and the chest wall, we will call PIP. Remember even at rest, we've got two opposing forces. We have the recoil of the lung. That's what's represented right here. And then the chest wall also has its own recoil, so that it wants to expand. That means that on this pleural space, we have two opposing forces. This diagram shows that when both have a pressure of zero, then the intrapleural pressure is going to be negative because it has two forces pulling on it in opposite directions. So we can say, that the difference in the alveolar pressure and the intrapleural pressure is what determines lung volume. We'll see that in just a minute. The important thing, too, is that for the lung to stay open, the intrapleural pressure needs to be less than the alveolar pressure. It needs to be less. Even if it becomes equal, you will and an issue. This is what happens in a pneumothorax. For instance if you get stabbed or somehow poked, so that air enters that pleural sac, then the intrapleural pressure equals zero. That which means that it's equal to atmospheric pressure. That's called a Pneumothorax. You've got air in that plural sac. That will cause the lung to collapse. When the Intrapleural pressure equals atmospheric pressure, not only will the lung collapse but the chest wall will expand. This is because you've removed it from being held onto the pleural sac. You'll have both the lung collapse and the chest wall expand if you make this pressure equal to atmospheric pressure. Let's talk about then what happens through the ventilation cycle. We will start at the end of expiration. Where we've just exhaled. So now we've got the scenario that we just talked about, where the chest wall wants to expand, the lung wants to contract, and we have a normal Intrapleural pressure of negative three. As we inspire, just when we are starting to inspire, we are going to increase the force that the chest wall is exerting on the system. It is expanding. That will stretch the lung. It will have greater recoil, and so the intrapleural pressure will now be even more negative. [SOUND] Since it's more negative and we said that the difference between the alveolar pressure and the intrapleural pressure is what determined the lung size, then that's going to cause the lung to expand. As the lung expands it's going to be a greater volume with the same amount of air. According to Boyles Law that means now we have a negative pressure in the alveoli. The intrapleural pressure is still more negative, but now we have a negative pressure in the alveoli. This means we will have air flow in because the difference in the alveoli pressure and the atmospheric pressure determines the direction of air flow. In this next step, at the end of expiration, now we have made the chest wall even greater. Our intrapleural pressure is even more negative, our recoil of our lungs is even greater, because it is larger. So now we have an increase even more in the volume of the lung. At the end of expiration, after just a split second, then we will have equilibrated between the alveolar pressure and atmospheric pressure. So in between breaths, the pressures will equilibrate between the alveoli and the atmospheric pressure. Then we will start to expire, to exhale. This occurs when we relax the diaphragm. That means that the force that the chest wall produced to expand has now greatly reduced. And so, our intrapleural pressure will be less negative. Our lung will be smaller now. Since we've got the same amount of air in a smaller space, the pressure has increased in the alveoli. This means air will flow out. That's going to continue to happen till we get to the end of expiration. Now we're back to where we started from. Our intrapleural pressure is negative, but not that negative so our lungs size is not that large. We've had time for equilibration so that our alveolar pressure is zero. This is what I call the plastic lung. It demonstrates a lot of the principles that we've been talking about, in terms of the pressures that are occurring and changing during breathing. The black balloon is going to represent the lung. The air in the canister represents the Intrapleural space. If I pull on this latex at the bottom, then I'm going to make the volume inside the canister larger. This will decrease the pressure in the intrapleural space, which occurs during inhalation, and it's going to expand the lungs. So, as I make the air chamber larger, then the pressure will decrease. The lung is gonna follow. That's what we talked about, of the difference between the pressure inside the alveoli versus the intrapleural pressure determines the size of the lung. That's what's happening here. Decrease the intrapleural pressure, and the lung is going to expand. Increase it by making the chamber smaller, and the lung contracts in size. Remember we also talked about how it's important that the intrapleural pressure is always less than the pressure in the lung. If not then you will have the lung collapse, which is a pneumothorax. This also happens to people if they have fluid or air enter the intrapleural space. So when I remove this stopper, then the pressure in the chamber equalizes with atmospheric pressure which is the same pressure inside the balloon. You'll see how the balloon collapses. [NOISE] We now have a collapsed lung. So now we're going to consider resistance in the airways, what influences resistance, and then how that's going to affect airflow. So again, we're gonna have this same, equation that we used in the cardiovascular system, where the difference in the alveolar pressure, and the atmospheric pressure is what determines flow, and that we will have a large contribution from resistance. So we know that one of the most important things in resistance of these airway tubes is gonna be their diameter. The smaller the diameter, the greater the resistance in the tube. So flow will decrease. Consider the lung anatomy. The farther you go into the lung, the tubes diameters are smaller but you have more tubes, therefore cross sectional area is larger. That means that resistance will decrease as you enter the lung. We also talked a little bit about how lung volume is going to affect the diameter of the airways. When your lung is full, everything is stretched. The airways are not as compressed, and so resistance will be decreased. This can actually be used as a compensation for a lung disease. If it is hard to exhale, as in an obstructive lung disease, then you can kind of breathe at a greater lung capacity. This means your lungs are more inflated even when you're exhaling. It can be a compensation for certain lung diseases. As with the circulatory system, we're going to be able to control the diameter, particularly of bronchioles which have lots of smooth muscle. This enables us to control air flow. This is going to be in contrast to the circulatory system, where sympathetic stimulation causes relaxation of the bronchioles. This makes sense if you're doing flight or fight. You're going to want to be able to open up your airways, so that you can get air into the lungs. You're going to want them to open. In contrast to when you have parasympathetic stimulation, then that smooth muscle of the bronchiole is more constricted and contracted. And then we've talked about this a little bit, but we are going to talk about it a little bit more. The elastic recoil of the airways is going to be important. In diseases such as emphysema, where we have reduced elastic tissue, then we have increased compliance. But decreased recoil can affect flow. Since you've got less recoil by the lung, that means that the intrapleural pressure will be less negative. You've got less of one of those forces, that is making it negative. Therefore the airway diameter will be smaller, and the resistance will be higher. So, if you don't have that recoil, then that can affect the airways. That's what we're going to be talking about right now. This is particularly prominent when your really trying to force the air out quickly. So for instance, if you're trying to exercise, then you want to get the air out quickly, and then quickly inhale. This is called a forced exhalation. Force the air out quickly. In a normal person, that will cause the Intrapleural pressure to become positive, because you're really squeezing that pleural sac. However, it's still less than the aveolar pressure. We're not going to collapse the lung. We've got that good lung recoil, so the lung is going to really contract or get smaller, which is going to make that pressure increase. Then as air moves out of the respiratory system, the air pressure will drop because of the resistance of the tubes. The thing that would be worrisome is you want to make sure that the pressure in these tubes is at least equal, or less or greater, sorry, than the intrapleural pressure. Otherwise, the tube will collapse. So here when the air pressure finally does get below the intrapleural pressure, it's okay because it's in a structure like a bronchus, or the trachea where there's cartilage. So it's not going to collapse. This is in contrast to an obstructive lung disease, like emphysema, where we've lost some of our recoil. So that even though we have a high intrapleural pressure, because the lung has recoiling less, and it's getting smaller, less efficiently, we've produced a smaller alveolar pressure. It's closer to the intrapleural pressure. And then, we often are going to also have an increased resistance in the airways, so that we can also have a more rapid drop in pressure as air flows out. In this case, what we're seeing is we have this spot right here where we've got a pressure inside the airway that is less than intrapleural pressure. It happens to be in a portion of the system that doesn't have cartilage. What that means is we're gonna have compression at that spot if not collapse. So we'll get this state where we'll have dynamic compression, where the pressure will build up and open it, but then it'll fall again and we'll have this dynamic process of it opening and closing. Because of all these factors of less recoil on the lung, and higher resistance in the airways, that makes the pressure drop more quickly in areas where there isn't cartilage. So, we've talked about the differences in pressure that will determine airflow and lung size. Then we've talked about how airway resistance is going to increase even in a normal person during expiration. But during forced expiration, when your intrapleural pressures are going to become positive, small airways can become compressed, especially in diseased states, and then they could even collapse.
